ArticleJournal of neurophysiology2010
BDNF evokes release of endogenous cannabinoids at layer 2/3 inhibitory synapses in the neocortex.
Article in Journal of neurophysiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 72 citations in OpenAlex.
- The endocannabinoidome-gut microbiome-brain axis as a novel therapeutic target for autism spectrum disorder.Journal of biomedical science · 2025Review
- Maladaptive changes in the homeostasis of AEA-TRPV1/CB1R induces pain-related hyperactivity of nociceptors after spinal cord injury.Cell & bioscience · 2025Article
- Selective alterations of endocannabinoid system genes expression in obsessive compulsive disorder.Translational psychiatry · 2024Article
- Article
- Brain-derived neurotrophic factor is a regulator of synaptic transmission in the adult visual thalamus.Journal of neurophysiology · 2022Article
- Review
- BDNF Activates Postsynaptic TrkB Receptors to Induce Endocannabinoid Release and Inhibit Presynaptic Calcium Influx at a Calyx-Type Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Activation of tyrosine phosphatase PTP1B in pyramidal neurons impairs endocannabinoid signaling by tyrosine receptor kinase trkB and causes schizophrenia-like behaviors in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Molecular Correlates of Topiramate and GRIK1 rs2832407 Genotype in Pluripotent Stem Cell-Derived Neural Cultures.Alcoholism, clinical and experimental research · 2020Article
- Lights on Endocannabinoid-Mediated Synaptic Potentiation.Frontiers in molecular neuroscience · 2020Review
- Impact of Chronic BDNF Depletion on GABAergic Synaptic Transmission in the Lateral Amygdala.International journal of molecular sciences · 2019Article
- Article
- Endogenous cannabinoids mediate the effect of BDNF at CA1 inhibitory synapses in the hippocampus.Synapse (New York, N.Y.) · 2018Article
- Functional Relevance of Endocannabinoid-Dependent Synaptic Plasticity in the Central Nervous System.ACS chemical neuroscience · 2018Review
- Examining the effects of alcohol on GABAAlcohol (Fayetteville, N.Y.) · 2018Article
- Depolarizing, inhibitory GABA type A receptor activity regulates GABAergic synapse plasticity via ERK and BDNF signaling.Neuropharmacology · 2018Article
- Molecular mechanisms of experience-dependent maturation in cortical GABAergic inhibition.Journal of neurochemistry · 2017Review
- BDNF-induced endocannabinoid release modulates neocortical glutamatergic neurotransmission.Synapse (New York, N.Y.) · 2017Article
- Examining FKBP5 mRNA expression in human iPSC-derived neural cells.Psychiatry research · 2017Article
- Perspectives on the Role of Endocannabinoids in Autism Spectrum Disorders.OBM neurobiology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The neurotrophin brain-derived neurotrophic factor (BDNF) is a potent regulator of inhibitory synaptic transmission, although the locus of this effect and the underlying mechanisms are controversial. We explored a potential interaction between BDNF and endogenous cannabinoid (endocannabinoid) signaling because activation of type 1 cannabinoid (CB1) receptors potently regulates γ-aminobutyric acid (GABA) release and both trkB tyrosine kinase receptors and CB1 receptors are highly expressed at synapses in neocortical layer 2/3. Here, we found that the effects of BDNF at inhibitory cortical synapses are mediated by the release of endocannabinoids acting retrogradely at presynaptic CB1 receptors. Specifically, acute application of BDNF rapidly reduced the amplitude of inhibitory postsynaptic currents (IPSCs) via postsynaptic trkB receptor activation because intracellular delivery of the tyrosine kinase inhibitor K252a completely blocked the BDNF effect. Although triggered by postsynaptic trkB activation, BDNF exposure decreased presynaptic release probability, as evidenced by increases in the paired-pulse ratio and coefficient of variation of evoked responses. In addition, BDNF decreased the frequency but not the amplitude of action potential-independent miniature IPSCs and BDNF did not alter the postsynaptic response to locally applied GABA. These results suggest that BDNF induces the release of a retrograde messenger from the postsynaptic cell that regulates presynaptic neurotransmitter release. Consistent with a role for endocannabinoids as the retrograde signal, the effect of BDNF on IPSCs was blocked by CB1 receptor antagonists and was occluded by a cannabinoid receptor agonist. Furthermore, inhibiting endocannabinoid synthesis or transport also disrupted the BDNF effect, implicating postsynaptic endocannabinoid release triggered by BDNF.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.